Is antithrombotic therapy necessary in erysipelas?

Objectivе. To investigate changes in the hemostastic system and blood rheology during the progression of the infection process in patients with lower-limb and facial erysipelas and to provide a rationale for the expediency of replacement and/or antithrombotic therapy. Subjects and methods. Sixty patients with erysipelas were examined in terms of the extrinsic (prothrombin time, international normalized ratio) and intrinsic (activated partial thromboplastin time) pathways of coagulation; the degree of dysfibrinogenemia (thrombin time, functional fibrinogen activity, and D-dimer level); the count and functional activity of platelets (aggregation to ADP) and erythrocytes (aggregation to lanthanoids and protamine sulfate). Endothelial dysfunction was also estimated from the decreased athrombogenicity of the vascular wall endothelium (antithrombin III and protein C) and the increased adhesive properties of the endothelium (von Willebrand factor). The comparison groups comprised healthy volunteers (n = 32) and patients with an inflammation focus localized on the face (n = 24) and lower limbs (n = 36) in the course of the disease (on days 1-3, 4-6, 7-10 and 11-15), who were treated at Infectious Diseases Hospital Two, Moscow. Results. The proposition that lower-leg erysipelas is 3.9 times more frequently complicated by hemorrhagic manifestations than facial erysipelas has been confirmed by laboratory findings. In particular, a significant decrease in protein C levels was noted in the patients with an erysipelatous inflammatory focus on the legs and concomitant chronic venous insufficiency. There were increased D-dimer and decreased a 2-macroglobulin levels, suggesting the potent activation of proteolytic enzymes (plasmin, matrix metalloproteinases, neutrophil elastase), which can be one of the causes of bullae, erosions, and ulcerations in the erysipelatous focus on the lower extremities. Conclusion. There were signs of intravascular (latent) hemolysis, such as lower haptoglobin concentrations and higher indirect bilirubin and LDH levels in the blood; a change in the rheological properties of red blood cells - their increased deformability (aggregation with lanthanum chloride) and decreased elasticity (aggregation with protamine sulfate) as one of the main causes of DIC-like syndrome in erysipelas.

facial erysipelas, lower-limb erysipelas, latent hemolysis, DIC-like syndrome, erythrocyte aggregation, platelet aggregation, fibrinogen, D-dimer, antithrombin III, von Willebrand factor, haptoglobin, β-hemolytic streptococcus